To view a near object with single clear binocular vision one must focus for the appropriate distance to see the near object clearly (accommodation) and converge (turn the eyes inwardly) so that both eyes are pointing at the near object so that the images of the near object in each eye are superimposed and thus perceived as a single object.
In 1864 Donders stated that “The use of positive or negative glasses, even after the lapse of a few hours, has an influence on the range of accommodation of the emmetropic eye.” and thereby first noted the changeable relationship between accommodation and convergence. Today, proposed mechanisms or treatments to prevent myopia range include the application of spectacles and contact lenses, pharmacological treatments, biofeedback and vision training. The various methods have demonstrated varying levels of success.
More than a century later it was shown that suturing the eyelids closed in different animals induced eye growth. Probably the most convincing evidence for optical control of eye length was shown first using the chick eye model in 1988. Positive and negative power lenses were administered to chick eyes leading to compensatory eye growth due to optical blur induced by the lenses. During that time and in the following years strong evidence for compensatory blur driven eye growth or active emmetropization was accumulated.
This was furthermore supported by numerous studies on refractive error distribution in developing human eyes. e.g. 8, 9, 10. However strong evidence for a genetic component in myopia development (for a review, see Goldschmidt 2003) keeps the debate as to whether nature or nurture is the primary cause of myopia active.
One of the very early works concerned with environmental factors playing a role in the etiology of myopia was published by Tscherning in 1882. He underlined the close relationship between the amount of close work performed and the prevalence of myopia. In recent years, the connection between myopia and near visual tasks has been considered by some researchers to be the most important environmental risk factors for myopia development. The relationship between the best retinal image plane during near tasks and the state of accommodation was thought to provide clues to eye growth. Functional hyperopic blur during near work (demonstrated by lag of accommodation) was thought to be the cue that triggers myopia progression. The first large scale controlled clinical trial using progressive spectacle lenses in school children that received a lot of attention in the scientific community was conducted in the United States and was based on a theory formulated in 1993. Increased lag of accommodation due to a reduced sensitivity to blur was thought to induce hyperopic blur during close work which in turn was assumed to induce eye growth due to functional hyperopia in school children. U.S. Pat. No. 6,343,861 describes specific progressive spectacle lens designs to slow the progression of myopia. Results of the clinical trial published in 2005, however, only showed very limited clinical benefit and this clinical benefit only arose in a particular subgroup of the study population, namely esophores.
An alternative to the accommodation lag hypothesis represents the work on peripheral refraction. The study showed impressive results in infant monkeys as to how the peripheral retina contributes to emmetropization even in the presence of unrestricted central vision. The treatment method based on these findings was published earlier that year in U.S. Published Pat. App. No. 20050105047[1]. While, subsequently, the same group of researchers and others have described various treatment methods based on this proposed mechanism, initial results of clinical trials have merely shown greater success compared with the findings from previous trials.
A very interesting aspect, which was largely ignored by the research community on peripheral refraction, was added by Flitcroft in 2006. He extended the concept of defocus to the three dimensional space during far and near visual tasks. The relative hyperopic defocus that can be shown in the peripheral retina would largely be reversed during most near visual tasks in which the highest stimulus to accommodation, for example a book or computer, is usually located in the central visual field while accommodation stimuli surrounding the near visual stimulus are much smaller. Therefore, the underlying mechanism thought to be responsible for myopia progression, is not apparent during those visual tasks that have been widely associated with myopia.
An early hypothesis and a treatment method looking into the potential effects of optical higher-order aberrations and myopia progression were presented in 1995 and described in U.S. Pat. No. 6,045,578. According to this theory, a shift of spherical aberration from positive values at distance to negative values at near focus produces a cue to eye growth because paraxial rays and marginal rays entering the eye do not share a common point of focus. Similar correcting designs to control myopia were also described, while others focused on the prevention of certain spatial frequencies to slow myopia progression. U.S. Pat. App. No. 20080084534A1 proposes a lens design with vertical coma aberration for presbyopia correction and simultaneous myopia prevention. A different higher order aberration mechanism for myopia control, based on lid force induced corneal distortions during reading, is described in U.S. Pat. No. 20060884425.
Others have proposed treatment methods that were based on aberration neutralization for the control of myopia. However to date, no studies have been published for any of these proposed methods that show a clinically significant treatment effect.
U.S. Pat. No. 6,752,499[1] describes a myopia treatment method, using commercially available bifocal contact lenses, for patients who also exhibit near point esophoria. The bifocal contact lens prescription add power is based on the patient's individual near point fixation disparity. The results presented are striking, showing an almost complete arrest of myopia progression in this population compared with single vision spectacles, single vision contact lenses and even progressive spectacle lens control groups. The disadvantage of the methodology is that the myopic population to be treated must also have some form of near point esophoria or fixation disparity. No treatment method is provided for progressing myopes without esophoria.
Another aspect of the prior art presents a treatment method for patients who also exhibit near point esophoria. U.S. Pat. No. 6,752,499[1] states that: “ . . . , the myopigenic effects of accommodation lag during intensive near work and hyperopic defocus are addressed by treating patients who suffer from near point esophoria” and: “ . . . add powers were individually chosen to maximally reduce the amount of near point associated esophoria.” This explanation does not take into account the multifocality of the optical lens design with respect to the associated hyperopic defocus induced in this population.
For a myopic patient with normal accommodation and convergence function the add power prescription while viewing a far distant target, induces a simultaneous second image that can be viewed as myopic stimulus inside the eye, therefore inhibiting myopia progression. The same myopic patient is expected to still use the distance prescription part of the lens design during close distance visual tasks due to the normal accommodative convergence to accommodation ratio. Thereby the retina is presented with a myopic stimulus of the add power part of the lens design during near visual tasks. The myopic subject uses the bifocal lens design not as it is intended for presbyopic patients that have no accommodation left. Instead normal accommodation is maintained and thereby a constant myopic stimulus during near and far distances viewing is present. Even in case of accommodative lag during near viewing one image is presented behind the retina while a second image is presented in front of the retina, which does not induce a clear stimulus to eye growth. According to the hyperopic blur stimulus hypothesis, this optical design should prevent myopia progression since a constant myopic blur stimulus is apparent. However prevention of myopia progression in myopes without near point esophoria was not shown.
In contrast, U.S. Pat. No. 6,752,499[1] discloses a treatment method applied to a study group of myopes with near point fixation disparity. The treatment method specifically intends to compensate for the fixation disparity (convergence without accommodation) with the near add power of the contact lens. Therefore, the population discussed in the '499 patent would use the bifocal lens design in the same way that a presbyopic patient would. They would use the distance zone of the bifocal lens for distance viewing and the near add power for near viewing.
In this context, hyperopic blur acts as a trigger to eye growth. The secondary image of the distance zone of the bifocal lens design induces hyperopic blur during near visual tasks, in this study population, yet prevents myopia progression according to U.S. Pat. No. 6,752,499[1]. Therefore, the theoretical mechanism assumed to cause myopia progression (i.e. hyperopic blur) appears to be wrong based on these results. Thus, there is still room for improvement in the field of myopia prevention and treatment by optical intervention.